Tuesday, May 13, 2008
Researchers Say Multiple Sclerosis in Childhood Is Linked to Lower IQ Scores
By Kelli Miller Stacy
WebMD Medical News Reviewed by Louise Chang, MD
May 12, 2008 -- Multiple sclerosis (MS) that strikes during childhood may disrupt a key phase of brain development and appears to have a profound negative impact on a child's ability to think and pay attention.
Scientists reporting in the May 12 issue of Neurology say that the earlier MS develops, the more likely a child will have a lower IQ score.
MS is a central nervous system disease that attacks myelin, the material that covers and protects nerve fibers. The damage gets worse over time and leads to symptoms such as numbness, tingling, fatigue, loss of vision, and in severe cases, paralysis.
It most commonly develops in adults after age 20. However, pediatric MS affects about 8,000-10,000 people under age 18 in the U.S., according to the National Multiple Sclerosis Society.
Researchers theorize that pediatric MS strikes at a time when the part of the brain involved in cognition is maturing. Previous uncontrolled studies have shown a link between cognitive impairment and MS. However, information about the neuropsychological effects of MS in children and teenagers has been limited.
"It's possible that MS can show an even more dramatic effect on the thinking skills and intelligence in children than in adults, since the disease might affect the brain at a time when it is still developing," researcher Maria Pia Amato, MD, of the University of Florence in Italy, states in a news release.
Amato gave an array of intelligence tests to 63 children with MS and compared their scores to 57 healthy children of similar ages. The tests were designed to measure overall intelligence, memory, language ability, and other thinking skills.
The tests showed that the children with MS were more likely to have low intelligence scores and problems with memory, attention, and other thinking skills. Thirty-one percent of the children with MS met the criteria for significant cognitive impairment, meaning they failed at least three of the tests. Fifty-three percent of the children with MS failed at least two of the tests.
Amato's team noted language difficulties in about 30% of the children with MS. Language problems are uncommon in adults with the disease.
"Since the disease occurs during a critical phase for language development, children may be particularly vulnerable to language problems," Amato states. "Even subtle language difficulties are likely to have important functional consequences. Therefore ... assessment of language function in pediatric MS deserves particular attention in future studies," she writes in the journal article.
© 2008 WebMD, LLC. All rights reserved.
By LOIS BAKER
A new multiple sclerosis study conducted by UB neurologists has shown that in addition to affecting women two-to-three times more than men, multiple sclerosis (MS) damages different regions of the brain in men and women.
The differences were defined by analyzing brain scans of 795 MS patients and 101 healthy controls using conventional magnetic resonance imaging (MRI) techniques, plus more advanced nonconventional MRI techniques, such as diffusion weighted imaging and magnetization transfer imaging.
Results of the study were presented recently at the annual meeting of the American Academy of Neurology.
The research showed that MS in women results in more atrophy of the brain’s white matter, the network of nerves that transport messages to the various brain regions, while the condition in men appears to cause more atrophy in the brain’s gray matter, the regions where messages are received and interpreted.
Ronald Antulov is first author on the study. He conducted the research while a neuroimaging fellow at the Buffalo Neuroimaging Analysis Center (BNAC), part of the Jacobs Neurological Institute, which is the Department of Neurology in the School of Medicine and Biomedical Sciences.
Antulov and colleagues examined consecutively 620 female and 175 male MS patients who were seen at the institute and compared scans with those of the healthy controls. All were assessed using conventional and nonconventional MRI measures.
“We found that atrophy of gray matter and central brain regions was more advanced in men, while atrophy of white matter was more advanced in women,” said Antulov. The phenomenon was not observed in healthy controls.
“We think these changes are influenced by a decrease in sex hormones,” Antulov said. “A recent study showing that male MS patients receiving testosterone treatment showed a lower rate of brain volume decline supports this concept. This finding also suggests that higher levels of estrogen may protect women against more severe MS-related brain damage.”
The BNAC is applying for grants to extend this research.
Contributing to the study, all from the BNAC-JNI, were Bianca Weinstock-Guttman, Jennifer Cox, Sara Hussein, Jackie Durfee, Michael Dwyer, Niels Bergsland, Nadir Abdelrahman, Milena Stosic, David Hojnacki, Frederick E. Munschauer and Robert Zivadinov.
The study was conducted in collaboration with the University of Rijeka, Croatia. Vladimir Miletic of that university also contributed to the research.
By John Gever, Staff Writer, MedPage Today
Published: May 01, 2008
Reviewed by Dori F. Zaleznik, MD; Associate Clinical Professor of Medicine, Harvard Medical School, Boston.
GRONINGEN, The Netherlands, May 1 -- The antidepressant drug fluoxetine (Prozac) curbed progression of relapsing-remitting multiple sclerosis in a small placebo-controlled study, but the effect lasted only a few months, researchers here said.
After 16 weeks of double-blind treatment, patients taking 20 mg/day of fluoxetine showed significantly fewer new lesions in MRI scans compared with patients receiving placebo, reported Jop P. Mostert, M.D., of the University of Groningen, and colleagues, online in the Journal of Neurology, Neurosurgery, and Psychiatry.
Twelve of 19 fluoxetine-treated patients had no new gadolinium-enhancing lesions at the 16-week evaluation, compared with five of 19 in the placebo group (P=0.02), they said.
However, the treatment phase lasted 24 weeks, and most measures of disease activity showed no significant differences between the fluoxetine and placebo groups at the study's final evaluation.
Still, the researchers wrote, "the results of our exploratory trial are sufficiently encouraging to justify further studies with fluoxetine in patients with multiple sclerosis."
They recommended that future trials use a higher fluoxetine dose combined with immunomodulating drugs.
The study was prompted by in vitro research and animal experiments suggesting that fluoxetine can modulate the activity of astrocytes, a class of immune cells in the brain, working to elevate cAMP signaling in these cells.
Astrocytes are involved in antigen-presentation and are thought to play a role in multiple sclerosis. They also carry serotonin receptors and reuptake sites, suggesting that serotonin reuptake inhibitors such as fluoxetine could reduce their activity.
Dr. Mostert and colleagues recruited 40 patients with established relapsing-remitting or relapsing secondary progressive multiple sclerosis who did not have a depression diagnosis. The mean time from first MS symptoms was 11 years.
Patients had no contraindications for repeated MRI scans or recent history of corticosteroids or immunomodulating drug therapy.
Participants were evaluated clinically and with MRI scans at baseline and at treatment weeks 4, 8, 16, and 24. One patient in each group discontinued prematurely, leaving 19 in each group for efficacy analysis.
At week 16, the mean cumulative number of new gadolinium-enhancing lesions -- the study's primary endpoint -- was 1.21 among fluoxetine-treated patients and 3.16 in the placebo group (P=0.05).
In addition to the larger number of patients showing no new lesions at 16 weeks, fluoxetine treatment was also associated with a smaller number of total scans showing new lesions (24% versus 47%, P=0.03).
Impressive-seeming numerical differences between groups remained at week 24, but the statistical significance largely vanished.
For example, the mean number of new enhancing lesions at week 24 was 1.84 in the fluoxetine group and 5.16 in the placebo group (P=0.15).
In the fluoxetine group, 32% of patients showed no new enhancing lesions at week 24, versus 21% of the placebo group (P=0.71).
Mean cumulative volume of new lesions at week 24 was 124 mm3 in the fluoxetine patients and 398 mm3 in the placebo group (P=0.16).
The only significant difference at week 24 was in the number of scans showing new lesions (25% in the fluoxetine group, 41% of the placebo group, P=0.04).
The number of patients having exacerbations and the total number of exacerbations did not differ noticeably between the fluoxetine and placebo groups.
Significantly more patients in the fluoxetine group reported nausea (65% versus 30% in the placebo group, P=0.03).
Other adverse effects did not differ significantly between groups, although 55% of fluoxetine patients reported drowsiness compared with 30% of those taking placebo.
The researchers noted that their small sample size limited the study's ability to detect significant treatment effects.
Nevertheless, they concluded, the results support their hypothesis about the role of cAMP signaling in astrocytes and its effect on inflammatory activity in multiple sclerosis.
The researchers added that fluoxetine may have other beneficial effects relevant to multiple sclerosis. For example, other studies have suggested it may help ward off axonal loss by stimulating release of neurotrophic factors.
The study was supported by Multiple Sclerosis anders [sic]. The researchers declared no potential conflicts of interest.
Primary source: Journal of Neurology, Neurosurgery and Psychiatry
Mostert J, et al "Effects of fluoxetine on disease activity in relapsing multiple sclerosis: A double-blind, placebo-controlled, exploratory study" Journal of Neurology, Neurosurgery, and Psychiatry 2008; DOI: 10.1136/jnnp.2007.139345
Merck Serono Announces Initiation of Phase II Clinical Trial of Atacicept in Relapsing Multiple Sclerosis
Geneva, Switzerland, April 30, 2008 – Merck Serono, a division of Merck KGaA, Darmstadt, Germany, and its partner ZymoGenetics, Inc. (NASDAQ: ZGEN) today announced the initiation of a Phase II clinical trial to evaluate the safety and efficacy of atacicept in patients with relapsing multiple sclerosis (RMS).
“This trial with atacicept underlines Merck Serono’s long-term commitment to patients with multiple sclerosis,” said Dr. Anton Hoos, Head of Global Development at Merck Serono. “Atacicept has the potential to complement existing MS drugs by offering a novel mode of action and convenient administration.”
“Patients with multiple sclerosis need more treatment options,” said Nicole Onetto, M.D., Senior Vice President and Chief Medical Officer of ZymoGenetics. “Our preclinical models have shown biological activity of atacicept in multiple sclerosis and, because of the growing body of supporting data in the literature indicating the importance of B cells and antibodies in the pathology of multiple sclerosis, we believe there is strong rationale for the clinical testing of atacicept in patients with RMS.”
The four-arm randomized, double-blind, placebo-controlled, multicenter study will evaluate the safety and efficacy of atacicept in patients with RMS over 36 weeks of treatment. The primary objective of the study is to evaluate the efficacy of atacicept in reducing central nervous system inflammation in subjects with RMS as assessed by frequent MRI measures.
Approximately 300 RMS patients meeting the eligibility criteria will be randomly assigned to receive one of three subcutaneous doses of atacicept or placebo for 36 weeks. Patients will be followed up until week 48.
Merck Serono and ZymoGenetics are developing atacicept (formerly referred to as TACI-Ig) as a potential treatment of autoimmune diseases, such as systemic lupus erythematosus (SLE), lupus nephritis (LN), rheumatoid arthritis and multiple sclerosis, as well as B-cell malignancies.
Atacicept contains the soluble TACI receptor that binds to the cytokines BLyS and APRIL. These cytokines are members of the tumor necrosis factor family that promote B-cell survival and autoantibody production associated with certain autoimmune diseases such as systemic lupus erythematosus. Current data indicates that levels of BLyS and APRIL are elevated in patients with rheumatoid arthritis, lupus erythematosus, B-cell malignancies and multiple sclerosis. Atacicept has been shown to affect several stages of B-cell development and may inhibit the survival of cells responsible for making antibodies.
About Merck Serono and multiple sclerosis
Merck Serono is a leader in multiple sclerosis (MS) with Rebif® (interferon beta-1a), a disease-modifying drug used to treat relapsing forms of MS, which is registered in more than 80 countries worldwide. In addition to Rebif®, the Company also offers a second therapy within its US portfolio of MS therapies: Novantrone® (mitoxantrone for injection concentrate) for worsening forms of MS. Full prescribing information for these products can be obtained by contacting the Company or visiting its website. Additional therapeutic options are currently under development at Merck Serono, including oral cladribine, currently in Phase III and potentially the first oral therapy for MS, as well as several products in early stage development. Merck Serono also is taking a leading role in developing an understanding of the role of genetics in MS.
About multiple sclerosis
Multiple sclerosis (MS) is a chronic, inflammatory condition of the nervous system and is the most common, non-traumatic, neurological disease in young adults. The World Health Organization estimates that up to 2.5 million people suffer from MS worldwide. While symptoms can vary, the most common symptoms of MS include blurred vision, numbness or tingling in the limbs and problems with strength and coordination. The relapsing forms of MS are the most common.
About Merck Serono
Merck Serono is the division for innovative prescription pharmaceuticals of Merck, a global pharmaceutical and chemical group. Headquartered in Geneva, Switzerland, Merck Serono discovers, develops, manufactures and markets innovative small molecules and biopharmaceuticals to help patients with unmet medical needs. Its North American business operates in the United States and Canada as EMD Serono.
Merck Serono has leading brands serving patients with cancer (Erbitux®), multiple sclerosis (Rebif®), infertility (Gonal-f®), endocrine and cardiometabolic disorders (Glucophage®, Concor®, Saizen®, Serostim®), as well as psoriasis (Raptiva®).
With an annual R&D investment of around € 1bn, Merck Serono is committed to growing its business in specialist-focused therapeutic areas including neurodegenerative diseases, oncology, fertility and endocrinology, as well as new areas potentially arising out of research and development in autoimmune and inflammatory diseases.
Merck is a global pharmaceutical and chemical company with total revenues of EUR 7.1 billion in 2007, a history that began in 1668, and a future shaped by 31,681 employees in 60 countries. Its success is characterized by innovations from entrepreneurial employees. Merck's operating activities come under the umbrella of Merck KGaA, in which the Merck family holds an approximately 70% interest and free shareholders own the remaining approximately 30%. In 1917 the U.S. subsidiary Merck & Co. was expropriated and has been an independent company ever since.
For more information, please visit www.merckserono.net or www.merck.de
Apr 29, 2008 - 4:38:53 PM
(HealthNewsDigest.com) - ST. LOUIS – Researchers at Saint Louis University are preparing to test an investigational pill to treat relapsing-remitting multiple sclerosis, the most common form of the potentially disabling neurological disease.
There are currently no oral medications approved to treat MS, which affects some 400,000 people in the United States (with approximately 10,000 new cases diagnosed each year). There are various medications to slow or modify the progression of the disease, but all must be injected into the skin, muscle or veins, making the search for an oral medication a top priority.
SLU will be one of several dozen sites around the world where researchers will study how patients with relapsing-remitting MS respond to the experimental drug laquinimod, which is taken in tablet form once a day. About 1,000 patients will be enrolled worldwide.
MS is a disease in which the body’s immune system attacks the protective coating – called myelin – surrounding the nerves within the central nervous system, as well as the nerve fibers themselves. Symptoms can vary widely from person to person, but they generally include fatigue, muscle weakness, numbness, impaired mobility, balance and cognition and vision disturbances.
About 85 percent of people newly diagnosed with the disease have relapsing-remitting MS. This form of the disease is characterized by periodic attacks or flare-ups (relapses), followed by months or even years of little to no signs of the disease (remission).
“Laquinimod seems to modulate how the immune system works,” said Florian P. Thomas, M.D., Ph.D., professor of neurology at the Saint Louis University School of Medicine and the study’s principal investigator. “In smaller, earlier trials, the drug reduced the likelihood of relapses in patients, as well as the number of MS lesions seen on MRI tests.”
In the randomized, double-blind study – the largest such investigation of the drug to date – half the volunteers will receive laquinimod while the remainder will be given a placebo.
They’ll remain in the trial for up to 30 months, during which time researchers will periodically assess how their disease develops. At various visits throughout the trial, patients will be given complete physical and neurological examinations, as well as an MRI scan to determine the extent of scarring on the brain – a defining characteristic of multiple sclerosis.
For the study, SLU researchers are looking for patients with relapsing-remitting MS between the ages of 18 and 55. Among other criteria, patients must not have taken any immuno-suppressive drugs within the last six months. Women must not be pregnant or breast feeding, and those of child-bearing age must be on at least two forms of birth control.
People wanting more information or to find out whether they qualify to participate in the study should call 314-977-4900.
Established in 1836, Saint Louis University School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: cancer, liver disease, heart/lung disease, aging and brain disease, and infectious disease.
© Copyright by HealthNewsDigest.com
04/28/2008 at 07:30 AM
MorphoSys AG (FSE: MOR; Prime Standard Segment, TecDAX) today announced the completion of a first dosing regimen in a phase 1 clinical study on healthy volunteers of the HuCAL-derived antibody MOR103 with no adverse events reported. Six healthy volunteers in the first dosing group have been enrolled and received MOR103 injections, while three volunteers received placebo. The safety review of the medical data from the lowest dosing group yielded a determination that it was safe to proceed with the second dosing group. The randomized, double-blind, placebo-controlled, single-ascending dose trial will be conducted in approx. 50 healthy volunteers and is being conducted in a Clinical Pharmacology Unit (CPU) in Utrecht, the Netherlands. The trial is scheduled to be finalized in 2008 and final reporting is expected in Q1 2009.
The Company's lead development program, MOR103, is a fully human HuCAL antibody directed against GM-CSF (granulocyte macrophage-colony stimulating factor), being developed in the area of inflammatory diseases, such as rheumatoid arthritis, where current treatment options are inadequate. Due to its diverse functions in the immune system, GM-CSF can be considered a target for a broad spectrum of anti-inflammatory therapies. MorphoSys had submitted the clinical trial application in December 2007 and received the approval by the Dutch authorities six weeks later. The study will evaluate the safety and tolerability as well as pharmacokinetics of escalating doses of MOR103.
"We are very pleased to see our first proprietary drug candidate progress according to plan," commented Dr. Marlies Sproll, Chief Scientific Officer of MorphoSys AG. "Antibodies that neutralize GM-CSF could represent a new generation of medicines that reduce inflammation with greater beneficial effects."
For further information please contact: Dr. Claudia Gutjahr-Löser, Head of Corporate Communications & Investor Relations, Tel: +49 (0) 89 / 899 27-122, email@example.com or Mario Brkulj, Manager Corporate Communications & Investor Relations, Tel: +49 (0) 89 / 899 27-454, firstname.lastname@example.org
MorphoSys is a publicly traded biotechnology company focused on the generation of fully human antibodies as a means to discover and develop innovative antibody-based drugs against life-threatening diseases. MorphoSys's goal is to establish HuCAL as the technology of choice for antibody generation in research, diagnostics and therapeutic applications. The Company currently has therapeutic and research alliances with the majority of the world largest pharmaceutical companies including Boehringer Ingelheim, Centocor/Johnson & Johnson, Novartis, Pfizer and Roche. Within these partnerships, more than 50 therapeutic antibody programs are ongoing in which MorphoSys participates through exclusive license and milestones payments as well as royalties on any end products. Additionally, MorphoSys is active in the antibody research market through its AbD Serotec business unit. The business unit has operations in Germany (Munich), the U.S. (Raleigh, NC) and U.K. (Oxford). For further information please visit http://www.morphosys.com/
About MOR103 to treat RA:
Rheumatoid arthritis (RA) is traditionally considered a chronic, inflammatory autoimmune disorder that causes the immune system to attack the joints and affects in particular a membrane, called synovium, which lines each movable joint. It is a disabling and painful inflammatory condition, which can lead to substantial loss of mobility due to pain and joint destruction. As a systemic disease, RA often affects extra-articular tissues throughout the body including the skin, blood vessels, heart, lungs, and muscles. The disease affects approximately 4-6 million people worldwide. In patients suffering from RA, white blood cells move from the bloodstream into the synovium. Here, these blood cells appear to play an important role in causing the synovial membrane to become inflamed. The HuCAL-based antibody MOR103 targets GM-CSF as a means to treat inflammatory diseases such as psoriasis, multiple sclerosis (MS), chronic obstructive pulmonary disease (COPD), asthma, and especially RA. The granulocyte macrophage colony-stimulating factor (GM-CSF) stimulates stem cells to produce granulocytes and macrophages, and subsequently activates these differentiated immune cells. GM-CSF is part of the natural immune and inflammatory cascade but has also been identified as an inflammatory mediator in autoimmune disorders like RA leading to an increased production of pro-inflammatory cytokines, chemokines and proteases and thereby ultimately to articular destruction. By neutralizing GM-CSF the HuCAL-based antibody MOR103 reduces undesired proliferation and activation of inflammatory granulocytes and macrophages and intervenes in several pathophysiological pathways. More information and picture material is available at: http://www.morphosys.com/en/mor103
HuCAL® and HuCAL GOLD® are registered trademarks of MorphoSys AG
This communication contains certain forward-looking statements concerning the MorphoSys group of companies. The forward-looking statements contained herein represent the judgment of MorphoSys as of the date of this release and involve risks and uncertainties. Should actual conditions differ from the Company's assumptions, actual results and actions may differ from those anticipated. MorphoSys does not intend to update any of these forward-looking statements as far as the wording of the relevant press release is concerned.
No strong evidence traumas like whiplash cause multiple sclerosis, B.C. Supreme Court rules
Saturday, April 26, 2008
A decade-long, $3-million lawsuit about whether a minor injury can trigger or exacerbate the onset of multiple sclerosis has collapsed after the B.C. Supreme Court ruled the underlying theory is likely bogus.
After hearing from the world's foremost neurological authorities, Justice Austin Cullen concluded in a recent pretrial ruling that medical consensus no longer considers trauma to be a potential catalyst of the disease linked to the body's auto-immune system.
The lengthy and complicated decision abruptly ended this specific suit, involving the Insurance Corporation of B.C., but it also may halt lots of other outstanding litigation launched across the continent on similar grounds -- the now-debunked hypothesis put forward by renowned researcher Dr. Charles M. Poser.
From the Harvard Medical School and a senior neurologist with the Beth Israel Deaconess Medical Centre, Poser has been a leading figure in multiple sclerosis research for decades. He is broadly published and highly respected.
Yet in the legal community, many blame him for creating a "courtroom problem driven by medical hogwash."
Justice Cullen came down on their side. He pummeled the octogenarian doctor for giving at times contradictory evidence, misinterpreting medical studies and slanting his testimony.
"Dr. Poser, who was the primary witness for the plaintiff, testified as an advocate for a theory that once had currency but has since been eroded by the advance of scientific studies and knowledge," the justice wrote.
"I found in his evidence a tendency to overstate the implications of studies that he relied on, and to be unduly dismissive of those that undermined his theory. While he has clearly achieved the status of a foremost expert in his field of neurology, I find that his commitment to his own theory of causation has to some extent impaired his objectivity and reliability as an expert witness."
Kirsten Mehl, lawyer for the winning side, was ecstatic: "I don't think he'll come back to our jurisdiction -- we got him!"
She blamed Poser's pet hypothesis for having set off a brush fire of litigation around the globe. At one point, U.S. court activity spurred the American Academy of Neurology to appoint a panel of specialists in an attempt to douse the conflagration and the National MS Society in 2003 was forced to weigh in, too.
"This theory only had a life in the courtroom," Mehl insisted. "He created the theory and gave evidence all over the world. That's why a lot of claims were brought and settlements were made."
It was cheaper for insurance companies to settle than go to court and risk that a judge would consider the medical evidence but still back an injured individual also suffering the debilitating effects of MS. That will change.
Besides listening to international authorities, Cullen reviewed more than 100 reports, studies and medical articles. His conclusion should put an end to litigation based on the belief minor trauma can exacerbate MS.
Lawyers in this case say dispelling Poser's opinion and aura was difficult and expensive.
That is in part because he was doing exactly what scientists are supposed to do -- posit a theory and examine the evidence. And, as you might expect, he enthusiastically and passionately defended his ideas.
But what is useful in one profession can disrupt another.
Poser's curiosity and conjecture were fine in the lab; in the courtroom, his research and analysis muddied the waters of liability by raising the rare possibility of causation. Cullen clarified the issue.
"This is the first case in Canada to really go into this situation in depth," said Robert Hartshorne, a lawyer for the defence. "It is the first North American case which analyses what has occurred here medically and it should put an end to these suits. You couldn't afford to do this every time this allegation came up. We brought in experts from the U.S., England, around the globe."
Opposing counsel Ronald Nairne agreed: "ICBC drew a line in the sand and threw everything at this. And they did very, very well. There were a number of cases like this out there and they won't proceed now."
This case has its roots in a minor fender-bender at the entrance to the SkyTrain parking lot on 10th Avenue on May 22, 1998. Both cars were only slightly damaged and were driven from the scene.
Later, driver Harris Taylor reported that as a result of the bump, she had strained the muscles in her right arm, suffered a twinge in her lower mid-back, and experienced a bit of agitation in her right shoulder. She had a history of lower-back problems.
On Sept. 8, 1998, she was diagnosed with MS at Vancouver General Hospital. The advanced stage of the disease supported the conclusion that it had been latent for some years before the accident. Nevertheless, at that time, there was a noisy debate over the controversial theory first proposed by Poser in the 1980s -- that minor trauma, whiplash or seemingly insignificant head injuries could bring on or exacerbate MS.
Back then, there was contemporaneous litigation under way in Australia, the U.S. and the U.K.
Nairne said a B.C. colleague had successfully handled a similar case here in 1995 that was settled out of court. It was thought Taylor had a similar claim that could be successfully pursued. She sued the owners of the other car -- Linda and Timothy Liong -- for more than $3 million in damages, most of which was associated with the MS claim.
At issue was whether, on a balance of probabilities, trauma could alter the natural course of the multiple sclerosis, and the lawsuit was fought as a "test case."
To answer the question, Justice Cullen embarked on a lengthy voir dire -- a trial within a trial --to determine the admissibility of expert evidence about the possible causal connection between trauma, including mild head trauma or whiplash injury, and the onset of symptomatic MS. He chose to hear specialists from both sides.
Surprisingly, Cullen was guided in his reasoning by a legal decision made in Scotland about the time this well-aged action was launched.
In that 1998 ruling on a similar suit, judge Lord Rodger concluded: "I do not find it proved, on a balance of probabilities, that trauma in general, or whiplash injury in particular, can trigger the onset of symptomatic MS . . . . I am not satisfied that whiplash injury can ever cause the onset of symptomatic MS."
Though it didn't bind him, Cullen found the reckoning behind the ruling "compelling by its lucid, careful and thorough analysis and conclusion. The fact that since that decision was pronounced (but not because of it) the relevant scientific community can be seen as coalescing around the scientific proposition that no causal relationship exists between trauma and MS symptoms in light of additional studies and discoveries, can only lend weight to the guidance implicit in Lord Rodger's extensive judgment."
Referring to study after study, Cullen averred: "All represent an erosion of support for the theory of a causal link between trauma and MS symptom onset within the medical world."
The idea that trauma could trigger the onset or exacerbation of MS symptoms is not a novel theory in the sense of being new. Researchers since at least the 1930s had suggested a link between an injury and the disease. Poser, however, had become its primary advocate -- the last man standing, if you will.
In 1999, the therapeutics and technology assessment sub-committee of the American Academy of Neurology published a "special article" written by a blue-ribbon panel that included Dr. William Sibley of the University of Arizona, Dr. George Ebers of the University of Western Ontario and Dr. Douglas Goodin, director of the MS Center at the University of California, San Francisco Medical Center. All of them testified before Justice Cullen.
Dr. Goodin said that the subcommittee was formed to conduct an assessment of the association between trauma and MS onset or exacerbation in response to a person who "felt that this [issue] was being misused in the courtroom."
Subsequently, in 2003, the National MS Society published its position referencing the AAN article and two separate epidemiological studies:
"Both studies showed that there are more traumatic events among people with MS than in the healthy control group. Many traumas were caused by MS symptoms such as incoordination, impaired balance, or abnormalities with gait or vision. These events, however, were not precipitating factors in the onset or exacerbation of the disease."
Recent medical texts also reflect that view: a complete reading of the literature provides no direct evidence in support of the hypothesis that trauma influences the expression or natural history of multiple sclerosis. Justice Cullen found the consensus compelling:
"I find that the likelihood of a causal connection between trauma and MS exacerbation is significantly less than that of a coincidental connection, in light of all the evidence adduced, and the opinion of a substantial majority of the scientific community. I thus conclude that even on a robust and pragmatic view of the evidence, it does not support proof of a causal connection between mild trauma, including whiplash, and MS exacerbation, on a balance of probabilities."
Which might put an end to the controversy in the courtroom, but it should do nothing to deaden the curiosity and enthusiasm of medical researchers -- no matter how esoteric or eccentric.
WHAT IS MULTIPLE SCLEROSIS?
B.C. Supreme Court Justice Austin Cullin provided the following sketch in his judgment of multiple sclerosis and its effects:
Multiple sclerosis is believed to be an autoimmune disease and that in North America, about one out of 1,000 people will be diagnosed with the affliction.
Another one in 1,000 will go undiagnosed despite having the condition.
Women were historically at double the risk of men.
Surprisingly and somewhat alarmingly, that ratio has changed dramatically (by an increase in incidence among women, rather than a decrease among men) in the past 50 years.
This strongly suggests environmental factors at play.
MS is characterized by the appearance of patches of inflammation associated with demyelination (loss of fatty insulation of nerve fibres) in the white matter of the brain, brain stem, optic nerve and spinal cord.
These patches, also called plaques or simply lesions, often occur in crops and they cause the common symptoms -- visual loss, double vision, numbness and/or weakness of the limbs.
The advent of magnetic resonance imaging (MRI) in about 1985 greatly aided researchers.
There is believed to be a strong genetic influence on the development of MS as studies have shown a relatively high correlation among family members.
Though environmental factors are also believed to be involved, they are as yet largely unidentified.
As to the triggers of the disease, epidemiological studies implicate viral infections as potential triggers in roughly 25 per cent of the cases.
There is no general acceptance of what other triggers may be responsible for the remaining 75 per cent of MS onset or exacerbation.
© The Vancouver Sun 2008